Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003873 (rheumatoid arthritis)
53,068 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In autoimmune disorders such as rheumatoid arthritis and systemic lupus erythematosus (SLE), autoantibodies are generated against a variety of macromolecules. Myositis is a human autoimmune disease characterized by weakness and wasting of muscle. In American studies, antibodies directed against soluble cellular constituents were detected by immunodiffusion in about 60% of cases; the commonest of these, found in 25% of patients, was antibody to the Jo-1 antigen. An antibody system referred to as PL-1 was recognized at a similar frequency in a series of patients studied at Hammersmith Hospital, London. We show here that this system is identical with the Jo-1 system and demonstrate that the antigen is a polypeptide of molecular weight (Mr) 50,000. The protein is immunoprecipitated with tRNA His and appears to be histidyl-tRNA synthetase. The identity of the Jo-1 antigen, the first of the RNA-associated antigens familiar in autoimmune disease to be characterized as a specific enzyme, suggests a model for virus involvement in autoantibody generation.
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PMID:Myositis autoantibody inhibits histidyl-tRNA synthetase: a model for autoimmunity. 686 13

The presence of autoantibodies to the Ro52 protein in sera from patients with idiopathic inflammatory myopathies has recently been reported. These antibodies were found predominately in sera with the myositis-specific autoantibody anti-histidyl-tRNA synthetase (anti-Jo-1). In this report, we analysed sera from 216 patients to determine whether anti-Ro52 antibodies are associated with myositis autoantibodies other than anti-Jo-1. These included sera containing antibodies that recognize threonyl- or alanyl-tRNA synthetases, Mi-2, PM-Scl, signal recognition particle (SRP), as well as the systemic sclerosis-related antibodies anti-topoisomerase I (Scl-70) and anti-centromere. A high proportion of sera that contain anti-aminoacyl-tRNA synthetase antibodies, anti-SRP, or anti-PM-Scl antibodies were found to contain antibodies to the Ro52 protein. In contrast, in sera containing anti-Mi-2, anti-Scl-70 or anti-centromere antibodies, anti-Ro52 antibodies were absent or occurred infrequently. In addition, only one serum from 41 rheumatoid arthritis patients was positive for anti-Ro52 autoantibodies. These data indicate that anti-Ro52 antibodies are produced in particular subsets of myositis patients, and are not limited to sera with anti-Jo-1 antibodies.
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PMID:The association of anti-Ro52 autoantibodies with myositis and scleroderma autoantibodies. 1004 34

The clinical significance of a discovery of anti-histidyl-tRNA synthetase (Jo1) autoantibodies patients was established in the early diagnosis of antisynthetase syndrome (ASS) as the common form of this pathology is characterized by interstitial lung disease (ILD), inflammatory muscle disease, and production of anti-Jo1 autoantibodies. However, the specificity of such autoantibodies has to be evaluated in daily clinical practice. In this study, the clinical and prognostic profiles of 45 patients displaying anti-Jo1 autoantibodies were determined. Among 36 patients with a titer of anti-Jo1 autoantibodies above the cutoff value suggested by the manufacturer (40 AU/mL), three different groups were identified. The first group (n = 26) suffered from a complete or incomplete ASS and showed anti-Jo1 autoantibodies mostly above 60 AU/mL. A second group (n = 7) suffered from another autoimmune disease, that is, a systemic lupus erythematosus, cutaneous lupus and rheumatoid arthritis, and Crohn's disease with anti-Jo1 autoantibodies mostly below 60 AU/mL. The third group (n = 3) did not suffer from any autoimmune disease and presented anti-Jo1 autoantibodies below 60 AU/mL. The nine doubtful cases (titer of anti-Jo1 autoantibodies of 30-39 AU/mL) were from patients with no ASS nor myositis. Only 27 out of 45 patients showed antinuclear antibodies with 15 sera showing a pattern characteristic of anti-Jo1 autoantibodies by indirect immunofluorescence on HEp2 cells. In conclusion, this study underlines the need to search for anti-Jo1 autoantibodies even if antinuclear antibodies are negative by indirect immunofluorescence and underlines the usefulness of anti-Jo1 antibodies of titer above 60 AU/mL in the diagnosis of complete or incomplete ASS.
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PMID:Clinical significance of anti-histidyl-tRNA synthetase (Jo1) autoantibodies. 1778 30

The immune system has evolved to eliminate or inactivate infectious organisms. An inappropriate response against self-components (autoantigens) can result in autoimmune disease. Here we examine the hypothesis that some evolutionarily conserved proteins, present in pathogenic and commensal organisms and their hosts, provide the stimulus that initiates autoimmune disease in susceptible individuals. We focus on seven autoantigens, of which at least four, glutamate decarboxylase, pyruvate dehydrogenase, histidyl-tRNA synthetase and alpha enolase, have orthologs in bacteria. Citrullinated alpha-enolase, a target for autoantibodies in 40% of patients with rheumatoid arthritis, is our main example. The major epitope is highly conserved, with over 90% identity to human in some bacteria. We propose that this reactivity of autoantibodies to shared sequences provides a model of autoimmunity in rheumatoid arthritis, which may well extend to other autoimmune disease in humans.
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PMID:Evolutionarily conserved antigens in autoimmune disease: implications for an infective aetiology. 1892 19

Rheumatoid arthritis (RA) and antisynthetase syndrome (ASS) are distinct clinical syndromes, and their co-occurrence is rarely encountered. The authors report the case of a 56-year-old female patient with RA of 3 years duration who suddenly developed ASS, and include a review of the literature. The patient was diagnosed with ASS based on; positivity for anti-histidyl-tRNA synthetase (Jo-1) antibody, interstitial lung disease, polyarthritis, and mechanic's hands. High-dose corticosteroid and pulse intravenous cyclophosphamide were used to control the ASS. This case demonstrates that ASS should be considered during clinical presentations due to its potential overlap with RA.
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PMID:Development of antisynthetase syndrome in a patient with rheumatoid arthritis. 2035 18